We determined whether chronic stress causes enduring hypertension and, if so, whether this is reflected in biochemical markers of sympathetic activity. Adult male Wistar rats were subjected to six weeks of footshocks (FS+, n=5), with constant monitoring of AP and HR by telemetry; another group served as controls (FS−, n=5). Chronic stress did not alter daily average values of AP or HR, mean AP being 122±1 and 116±2 mmHg for FS+ and FS−, respectively, post‐stress, vs. 120±3 and 119±3 mmHg, respectively, pre‐stress. Chronic stress failed to alter cardiac susceptibility to arrhythmias, and did not alter AT1 receptor expression or tyrosine hydroxylase activity in the stellate ganglia or the adrenal gland. However, chronic stress dramatically altered circadian rhythms, significantly disrupting the normal dark phase rises in AP and HR. These changes were already detectable after the first week of stress, and lasted for at least one week post‐stress. We conclude that chronic footshock stress does not provoke sustained changes in daily average values of AP or HR, or in biochemical markers of sympathetic activity, but causes enduring disruption of circadian rhythms.